Jakab G J, Risby T H, Hemenway D R
Department of Environmental Health Sciences, Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD 21205.
Res Rep Health Eff Inst. 1992 Oct(53):1-39, discussion 41-9.
Knowledge about the health effects of exposure to formaldehyde associated with automotive emissions is of pivotal importance in the risk assessment of this agent. Mobile sources emit many combustion-derived pollutants, including formaldehyde, in association with respirable carbon particles. Because it is hydrophilic, most of the inhaled formaldehyde is absorbed in the upper respiratory tract. However, if the organic vapor is adsorbed on respirable particles, formaldehyde may be deposited in the deep lung with the inhaled particles and may be available to interact adversely with cells along the lung parenchyma. On the respiratory surface, the alveolar macrophage phagocytic system plays the pivotal role in defending the lung against infectious agents. Susceptibility to respiratory infections is a relevant and sensitive indicator of the adverse effects of air pollution because acute and chronic exposures to a variety of air pollutants have been shown to decrease pulmonary antibacterial defenses. The goal of this research was to investigate whether exposure to formaldehyde decreases resistance to respiratory infections through dysfunctions of the alveolar macrophage phagocytic system. The study also explored whether interactions between formaldehyde and respirable carbon black particles alter susceptibility to respiratory infections and impairment of alveolar macrophage phagocytosis by delivering adsorbed formaldehyde to the deep lung with the inhaled particles. A carbon black, Regal GR, was used in these studies as a surrogate for the carbonaceous core of Diesel particulate matter. This material was selected to represent the worst-case scenario because the carbon black was expected to adsorb formaldehyde strongly. To accomplish this goal, mice were exposed to formaldehyde and to carbon black and formaldehyde combinations; increased susceptibility to respiratory infections was quantified by alveolar macrophage-dependent intrapulmonary killing of Staphylococcus aureus after an inhalation challenge with the bacterium. The salient findings of the bactericidal studies are as follows: Fifteen parts per million (ppm)* formaldehyde impaired the intrapulmonary killing of S. aureus when exposure followed the bacterial challenge. One ppm formaldehyde impaired the intrapulmonary killing of S. aureus when exposure preceded and was continued after the bacterial challenge. Coexposures to target concentrations of 3.5 mg/m3 carbon black and 2.5 ppm formaldehyde, or 10 mg/m3 carbon black and 5 ppm formaldehyde after the bacterial challenge had no effect on the intrapulmonary killing of S. aureus. Preexposure for four hours per day for four days to target concentrations of 3.5 mg/m3 carbon black and 2.5 ppm formaldehyde had no effect on the intrapulmonary killing of S. aureus when the assay was performed one day after the cessation of exposure.(ABSTRACT TRUNCATED AT 400 WORDS)
了解与汽车排放相关的甲醛暴露对健康的影响在该物质的风险评估中至关重要。移动源排放许多燃烧产生的污染物，包括甲醛，这些污染物与可吸入碳颗粒相关联。由于甲醛具有亲水性，吸入的大部分甲醛在上呼吸道被吸收。然而，如果有机蒸气吸附在可吸入颗粒上，甲醛可能会随着吸入颗粒沉积在深部肺部，并可能与肺实质中的细胞发生有害相互作用。在呼吸表面，肺泡巨噬细胞吞噬系统在保护肺部免受感染因子侵害方面起着关键作用。对呼吸道感染的易感性是空气污染不良影响的一个相关且敏感的指标，因为已表明急性和慢性暴露于多种空气污染物会降低肺部抗菌防御能力。本研究的目的是调查暴露于甲醛是否会通过通过肺泡巨噬细胞吞噬系统功能障碍而降低对呼吸道感染的抵抗力。该研究还探讨了甲醛与可吸入炭黑颗粒之间的相互作用是否会通过将吸附的甲醛与吸入颗粒一起输送到深部肺部而改变对呼吸道感染的易感性以及肺泡巨噬细胞吞噬作用的损害。在这些研究中，使用了一种炭黑Regal GR作为柴油颗粒物碳质核心的替代物。选择这种材料代表最坏情况，因为预计炭黑会强烈吸附甲醛。为实现这一目标，将小鼠暴露于甲醛以及炭黑与甲醛的组合中；通过在用金黄色葡萄球菌进行吸入攻击后，依赖肺泡巨噬细胞的肺内杀灭金黄色葡萄球菌来量化对呼吸道感染易感性的增加。杀菌研究的主要发现如下：百万分之十五（ppm）*的甲醛在细菌攻击后暴露时会损害肺内杀灭金黄色葡萄球菌的能力。百万分之一的甲醛在细菌攻击之前暴露并在攻击后持续暴露时会损害肺内杀灭金黄色葡萄球菌的能力。在细菌攻击后，同时暴露于目标浓度为3.5毫克/立方米的炭黑和2.5 ppm的甲醛，或10毫克/立方米的炭黑和5 ppm的甲醛，对肺内杀灭金黄色葡萄球菌没有影响。在停止暴露一天后进行测定时，每天暴露四小时，连续四天暴露于目标浓度为3.5毫克/立方米的炭黑和2.5 ppm的甲醛，对肺内杀灭金黄色葡萄球菌没有影响。（摘要截取自400字）
